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Beta Interactions

Lorenzo, A., Yuan, M., Zhang, Z., et al. (2000) Amyloid beta interacts with the amyloid precursor protein a potential toxic mechanism in Alzheimer s disease. Nat. Neurosci., 3, 460-464. [Pg.332]

Several lines of evidence show that there is a specific region in the intracellular loop between domains I and II of the a, subunit that serves as the primary site for binding of P subunits. This site has been named the alpha interaction domain (AID Pragnell et al., 1994). Cavps contain a beta interaction domain (BID) that, until very recently, was thought to serve as the primary site for interaction with the a, subunit (DeWaard et al., 1994). However, resolution of the structure of Ca2+ channel P subunits has indicated that such a view may be oversimplified. [Pg.273]

Kohn, A.B., Roberts-Misterly, J.M., Anderson, P.A.V., Khan, N. and Greenberg, R.M. (2003b) Specific residues in the beta interaction domain of a schistosome Ca2+ channel p subunit are key to its role in sensitivity to the antischistosomal drug praziquantel. Parasitology 127, 349-356. [Pg.280]

The Fermi and Gamow-Teller rules correspond respectively to the emission of an electron-neutrino pair in a singlet or triplet state. Convincing evidence has accumulated that transitions of the type 0->0, No and 0- 1, No both occur with high probability, so that the general beta-interaction may contain both scalar and tensor terms. [Pg.35]

Wu CS et al (1965) The experimental determination of the beta interaction. In Siegbahn K (ed) Alpha-, beta- and gamma-ray spectroscopy, vol 2. North-Holland, Amsterdam... [Pg.141]

The secondary elements interact as one would predict from their net charges. Helix-helix interactions are strongly repulsive, helix-Beta slightly attractive and Beta-Beta interactions clearly attractive, as one would expect from their H-bonding alignment. [Pg.37]

The Hamiltonian considered above, which connmites with E, involves the electromagnetic forces between the nuclei and electrons. However, there is another force between particles, the weak interaction force, that is not invariant to inversion. The weak charged current mteraction force is responsible for the beta decay of nuclei, and the related weak neutral current interaction force has an effect in atomic and molecular systems. If we include this force between the nuclei and electrons in the molecular Hamiltonian (as we should because of electroweak unification) then the Hamiltonian will not conuuiite with , and states of opposite parity will be mixed. However, the effect of the weak neutral current interaction force is mcredibly small (and it is a very short range force), although its effect has been detected in extremely precise experiments on atoms (see, for... [Pg.170]

S. Increased synthesis of transforming growth factor-beta , which blocks cell division and promote.s apoptosis by interacting with its own membrane recepror,... [Pg.285]

Similar to beta decay is positron emission, where tlie parent emits a positively cliargcd electron. Positron emission is commonly called betapositive decay. Tliis decay scheme occurs when tlie neutron to proton ratio is too low and alpha emission is not energetically possible. Tlie positively charged electron, or positron, will travel at higli speeds until it interacts with an electron. Upon contact, each of tlie particles will disappear and two gamma rays will... [Pg.194]

Despite the large number of molecules found to interact with the TGF- 3 pathway, few have been identified as functional tumor suppressors using either mouse or human genetics. The TGF-beta pathway is inactivated in nearly all gastrointestinal cancers, from TBRII, TBRI, Smad 2, and Smad 4. Recent exciting data have revealed the role of ELF, a key TGF- 3 pathway adaptor, in hepatocellular cancer suppression. [Pg.1231]

Because the path of the s process is blocked by isotopes that undergo rapid beta decay, it cannot produce neutron-rich isotopes or elements beyond Bi, the heaviest stable element. These elements can be created by the r process, which is believed to occur in cataclysmic stellar explosions such as supemovae. In the r process the neutron flux is so high that the interaction hme between nuclei and neutrons is shorter that the beta decay lifetime of the isotopes of interest. The s process chain stops at the first unstable isotope of an element because there is time for the isotope to decay, forming a new element. In the r process, the reaction rate with neutrons is shorter than beta decay times and very neutron-rich and highly unstable isotopes are created that ultimately beta decay to form stable elements. The paths of the r process are shown in Fig. 2-3. The r process can produce neutron-rich isotopes such as Xe and Xe that cannot be reached in the s process chain (Fig. 2-3). [Pg.19]

Weber LM, Hayda KN, Haskins K et al (2007) The effects of cell-matrix interactions on encapsulated beta-cell function within hydrogels functionalized with matrix-derived adhesive... [Pg.167]

In striated muscle, there are two other proteins that are minor in terms of their mass but important in terms of their function. Tropomyosin is a fibrous molecule that consists of two chains, alpha and beta, that attach to F-actin in the groove between its filaments (Figure 49-3). Tropomyosin is present in all muscular and muscle-fike structures. The troponin complex is unique to striated muscle and consists of three polypeptides. Troponin T (TpT) binds to tropomyosin as well as to the other two troponin components. Troponin I (Tpl) inhibits the F-actin-myosin interaction and also binds to the other components of troponin. Troponin C (TpC) is a calcium-binding polypeptide that is structurally and functionally analogous to calmodulin, an important calcium-binding protein widely distributed in nature. Four molecules of calcium ion are bound per molecule of troponin C or calmodulin, and both molecules have a molecular mass of 17 kDa. [Pg.562]

Cheng ZJ, Zhao J, Sun Y, Hu W, Wu YL, Cen B, Wu GX, Pei G (2000) Beta-arrestin differentially regulates the chemokine receptor CXCR4-mediated signaling and receptor internalization, and this implicates multiple interaction sites between beta-arrestin and CXCR4. J Biol Chem 275 2479-2485... [Pg.241]

Abraham S, Sweet T, Sawaya BE, Rappaport J, Khalili K, Amini S (2005) Cooperative interaction of C/EBP beta and Tat modulates MCP-1 gene transcription in astrocytes. J Neuroimmunol 160 219-227... [Pg.365]


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